中国部分甲肝病毒流行株结构蛋白VP3-VPl区基因特点分析

目的分析中国部分甲肝病毒流行株结构蛋白VP3-VPl区基因特点。方法收集42份甲肝患者急性期血清标本,经核酸提取、逆转录及巢氏PCR,测得结构一非结构蛋白VP3-VPl-2A区序列,进行序列同源性比较并分析其基因特点。结果42株HAV病毒株在VPl-2A连接处核苷酸和氨基酸序列同源性分别为89．1％～100％和97．3％～100％;在全长结构蛋白VP3-VPl区的核苷酸和氨基酸序列同源性分别为87．6％～100％和98．8％～100％。VPl-2A连接处序列相同的病毒株在全长结构蛋白VP3．VPl区的核苷酸同源性为98．4％～100％,0～2个氨基酸位点不同。本实验所得序列在中和抗原位点处氨基酸序列均未变异。结论42株病毒株均属于I型,40株是IA亚型,2株IB亚型。本实验所用HAV流行株在结构蛋白VP3．VPl区的核苷酸存在差异但是氨基酸序列高度保守且没有中和抗原位点处的变异。VPl-2A结合处核苷酸序列相同的分离株在全长结构蛋白VP3-VPl区核苷酸序列相同或相近,氨基酸序列保守。     

烟台市手足口病合并脑炎病毒分离及基因序列分析

目的 了解烟台地区手足口病合并脑炎病原谱及其基因学特征.方法 采集烟台地区手足口病合并脑炎患者粪便及脑脊液标本,通过细胞培养分离病毒,实时荧光PCR鉴定病毒型别,RT-PCR扩增VP1区基因部分序列并测序,进行序列分析.结果 10份粪便标本分离病毒3株,均为EV71.与C4a型代表株核苷酸同源性为98％～99％,氨基酸同源性98.90％～99.45％.系统发生树中,烟台分离株与C4亚型C4a簇代表株位于同一分支.结论 烟台地区手足口病合并脑炎病原主要为EV71,属于C4亚型C4a簇.     

惠州市重症手足口病病原谱及EV71型VP1区基因特征分析

目的分析惠州市手足口病重症病例的病原谱构成,了解惠州市肠道病毒71型分离株的VPl区基因特征．为科学防治手足口病提供科学依据。方法采集300例重症手足口病（HFMD）患者标本,采用实时荧光RT-PCR检测肠道病毒核酸,并对肠道病毒7l型（EV71）和柯萨奇病毒A16型（CoxA16）进行分型检测;选择8株EV71分离株进行VPl区基因全长序列测定,测序结果利用DNASTAR软件进行核苷酸、氨基酸序列分析和同源性比较。并用Mega5．0软件构建亲缘性进化树。结果通过实时荧光RT-PCR特异性检测,EV71阳性结果154份,阳性率为51．33％;CoxAl6阳性结果38份,阳性率为12．67％。测序结果表明,8株EV71之间的VPl基因核苷酸同源性为96．9％～99．2％。氨基酸同源性为99．3％～100％。VPI区基因遗传进化分析表明。8株EV71分离株与c4基因亚型的代表株处于同一分支,均属于C4基因亚型的C4a进化分支。结论惠州市手足口病疫情主要病原EV71病毒均属于C4a基因亚型,与2004年以来的中国大陆EV71病毒流行的基因型一致,未产生明显的抗原漂移及变异。     

青海省分离到肠道病毒71型及其VP1区基因特征分析

目的 研究2008年青海省手足口病（Hand,Foot and Mouth Disease,HFMD）的致病病原体中肠道病毒71型（Human Enterovirus 71,HEV71）的VP1区基因特征.方法 采集青海省HFMD患者的粪便、疱疹液和咽拭子标本共335份,并进行病毒分离,然后对阳性分离株病毒进行肠道病毒血清型别的分子定型.对分离到的HEV71阳性分离株进行VP1编码区基因扩增,核苷酸序列测定和同源进化分析.结果 在335份临床标本中,共分离到45株阳性病毒分离物,其中30株鉴定为HEV71（占66.7%）,是主要病原体.对30株HEV71进行VP1区核苷酸序列测定后,分析发现它们在VP1区核苷酸水平和氨基酸水平上有一定差异,同源性分别在95.2%～100.0%和96.6%～100%之间.它们与1998年以来在我国分离的HEV71在核苷酸和氨基酸水平上的同源性都较高.与其他35株各基因型和基因亚型的HEV71代表株构建的亲缘进化树中显示,青海省HEY71分离株与C4亚型代表株聚为一簇,属于C4基因亚型C4a进化分支.结论 青海省从HFMD病例中分离到HEV71,也确认了青海省HFMD的病原体HEV71流行株的基因型为C4基因型中的C4a进化分支,并且存在多个传播链.     

2009年深圳地区肠道病毒71型毒株VP4基因进化分析

目的 对深圳地区手足口病(hand,foot and mouth disease,HFMD)肠道病毒71型分离株(enterovirus 71,EV71)的VP4基因遗传进化进行分析.方法 2009年采集深圳市儿童医院就诊的HFMD患者的粪便标本491份,选取其中8份经细胞培养鉴定为阳性的EV71毒株用RT-PCR扩增VP4基因,利用MEGA4.0软件进行遗传进化分析.结果 2009年深圳地区8株EV71 VP4基因全长207 bp,编码69个氨基酸;8株EV71 VP4基因核苷酸同源性为94.2％ ～98.1％,与深圳2001至2004年分离的17株EV71毒株核苷酸同源性在89.9％ ～98.1％,与GenBank中其他EV71病毒株VP4的核苷酸同源性为79.2％～100％;其中与亚洲流行株阜阳株(EU703812)核苷酸的同源性最高(100％),其次是C4代表株及2004年深圳株(AY895144)为94.2％ ～97.1％.除了印度株和其中1株EV71的VP4编码的氨基酸在第54位(ACA)不同之外,其余7株EV71 VP4编码的氨基酸序列之间以及与GenBank报道的其他序列同源性达100％.8株EV71 VP4基因核苷酸与C4代表株相比有17处不同,除1处以外其余全在简并密码位点上;轻重症病例毒株之间VP4基因序列未见明显改变.进化树显示8株EV71均属于C4基因亚型.结论 2009年深圳市流行的EV71属于C4基因亚型,流行的EV71 VP4基因非常保守,不属于变异区段,绝大部分核苷酸的变异属无义突变,VP4基因编码的氨基酸变异几乎为0.     

重庆流行性乙型脑炎病毒分离株CQ11-66在PrM/C及E基因区的分子特征

目的 分析重庆地区儿童流行性乙型脑炎(简称乙脑)病毒分离株CQ11-66在PrM/C及E基因区的分子特征.方法 采集重庆医科大学附属儿童医院感染消化科诊断的流行性乙脑患者血液及脑脊液标本,通过接种BHK-21细胞检测并分离乙脑病毒,并对其PrM/C及E基因区测序.使用Clustal X(1.8)、MEGA5等生物学软件进行核苷酸序列、氨基酸序列及系统进化分析.结果 本研究仅从儿童乙脑患者脑脊液标本中分离到1株乙脑病毒,命名为CQ11-66.CQ11-66和其他国家及地区的乙脑病毒分离株相比,PrM/C基因区总体核苷酸及氨基酸序列同源性分别为74.8％～97.4％及85.6％～98.7％,而E基因区总体核苷酸及氨基酸序列同源性分别为81.6％ ～ 99.6％及94.8％ ～99.6％;CQ11-66株与福建省乙脑病毒人分离株相比较,在PrM/C、E基因核苷酸及氨基酸序列同源性均很高.基于PrM/C及E基因区核苷酸序列进行系统进化分析,CQ11-66株属于基因Ⅲ型.结论 在重庆市儿童乙脑患者标本中分离到1株乙脑病毒CQ11-66,CQ11-66株在PrM/C和F基因区核苷酸序列和氨基酸序列同其他乙脑病毒分离株存在一定的差异,且系统进化分析显示CQ11-66株属于乙脑病毒基因Ⅲ型.     

四川省流行性乙型脑炎病毒优势基因型的研究

目的了解四川省乙脑主要流行区乙脑病毒的分子生物学特性,为防治提供依据。方法对2007-2010年间分离到的13株乙脑病毒进行PreM和E基因区扩增,采用MEGA5生物学软件完成氨基酸序列和病毒进化树分析。结果基因分型显示13株均属于基因I型。13株病毒之间比较,PreM基因核苷酸和氨基酸同源性为97％-100％和98．7％-100％,E基因核苷酸和氨基酸同源性为97．8％～99．9％和99．6％～100％,其同源性极高。13株病毒与2004年四川分离株比较E基因核苷酸同源性在97．7％～99．6％之间,氨基酸同源性在98．6％-100％之间;PreM基因的核苷酸同源性在96．2％-99．1％之间,氨基酸同源性在97．5％-98．7％之间;与疫苗株P3和SA14—14—2比较E基因核苷酸和氨基酸同源性分别为87．6％～88．3％和97％～97．8％;PreM基因核苷酸和氨基酸同源性分别为84．1％～85．8％和93．7％-96．2％。13株病毒E基因的8个氨基酸毒力位点均没有发生改变。结论四川省乙脑病毒已呈现基因I型为优势型别的态势,其PreM和E区核苷酸和氨基酸高度保守,关键的氨基酸毒力位点没有变化,提示目前使用的疫苗对流行株的感染具有保护作用。     

中国部分甲肝病毒流行株结构蛋白VP3-VP1区基因特点分析

目的 分析中国部分甲肝病毒流行株结构蛋白VP3-VP1区基因特点.方法 收集42份甲肝患者急性期血清标本,经核酸提取、逆转录及巢氏PCR,测得结构-非结构蛋白VP3-VP1-2A区序列,进行序列同源性比较并分析其基因特点.结果 42株HAV病毒株在VP1-2A连接处核苷酸和氨基酸序列同源性分别为89.1%～100%和97.3%～100%;在全长结构蛋白VP3-VP1区的核苷酸和氨基酸序列同源性分别为87.6%～100%和98.8%～100%.VP1-2A连接处序列相同的病毒株在全长结构蛋白VP3-VP1区的核苷酸同源性为98.4%～100%,0～2个氨基酸位点不同.本实验所得序列在中和抗原位点处氨基酸序列均未变异.结论 42株病毒株均属于I型,40株是IA亚型,2株IB亚型.本实验所用HAV流行株在结构蛋白VP3-VP1区的核苷酸存在差异但是氨基酸序列高度保守且没有中和抗原位点处的变异.VP1-2A结合处核苷酸序列相同的分离株在全长结构蛋白VP3-VP1区核苷酸序列相同或相近,氨基酸序列保守.     

中国部分甲肝病毒流行株结构蛋白VP3-VP1区基因特点分析

目的 分析中国部分甲肝病毒流行株结构蛋白VP3-VP1区基因特点.方法 收集42份甲肝患者急性期血清标本,经核酸提取、逆转录及巢氏PCR,测得结构-非结构蛋白VP3-VP1-2A区序列,进行序列同源性比较并分析其基因特点.结果 42株HAV病毒株在VP1-2A连接处核苷酸和氨基酸序列同源性分别为89.1%～100%和97.3%～100%;在全长结构蛋白VP3-VP1区的核苷酸和氨基酸序列同源性分别为87.6%～100%和98.8%～100%.VP1-2A连接处序列相同的病毒株在全长结构蛋白VP3-VP1区的核苷酸同源性为98.4%～100%,0～2个氨基酸位点不同.本实验所得序列在中和抗原位点处氨基酸序列均未变异.结论 42株病毒株均属于I型,40株是IA亚型,2株IB亚型.本实验所用HAV流行株在结构蛋白VP3-VP1区的核苷酸存在差异但是氨基酸序列高度保守且没有中和抗原位点处的变异.VP1-2A结合处核苷酸序列相同的分离株在全长结构蛋白VP3-VP1区核苷酸序列相同或相近,氨基酸序列保守.     

临沂市脑膜炎／脑炎症候群监测病例埃可病毒30型的分离及其基因特征分析

目的 调查山东省临沂市脑膜炎/脑炎症候群（AMES）病例中人类肠道病毒病原谱的构成,分析主要病原体埃可病毒30型的基因特征.方法 采集AMES病例的脑脊液、粪便和（或）咽拭子标本,所有标本经预处理后,接种RD、Hep-2细胞分离病毒,阳性分离物采用血清学和分子生物学方法鉴定型别,与GenBank检索到的其他Echo30毒株进行同源性比较,并构建VP1完整编码区系统进化树研究其遗传进化规律.结果 2010年4-12月,共采集101例病例的222份标本（脑脊液56份,咽拭子94份,粪便72份）,其中34例患者的47份标本（脑脊液4份,咽拭子18份,粪便25份）中分离到HEV,11例鉴定为Echo30.通过同源性分析,发现其核苷酸同源性与2003年山东省泰安市、章丘市及江苏省分离株最近（91.2％～95.4％）,与原型株差异较大（17.9％～19.6％）;11株临沂分离株之间核苷酸差异为0～10.2％.系统进化树分析显示,临沂分离株属于基因型6的3个不同分支,提示来自3个传播链的Echo30病毒在临沂市共同循环.结论 山东省临沂市2010年AMES病例标本的优势分离株为Echo30,与国外分离株属于不同的进化分支,具有不同的基因特征.     

Opportunities and challenges in the prevention and control of cancer and other chronic diseases: children's diet and nutrition and weight and physical activity

OBJECTIVE: The purpose of this article is to review the role of behavioral research in disease prevention and control, with a particular emphasis on lifestyle- and behavior-related cancer and chronic disease risk factors--specifically, relationships among diet and nutrition and weight and physical activity with adult cancer, and tracking developmental origins of these health-promoting and health-compromising behaviors from childhood into adulthood. METHOD: After reviewing the background of the field of cancer prevention and control and establishing plausibility for the role of child health behavior in adult cancer risk, studies selected from the pediatric published literature are reviewed. Articles were retrieved, selected, and summarized to illustrate that results from separate but related fields of study are combinable to yield insights into the prevention and control of cancer and other chronic diseases in adulthood through the conduct of nonintervention and intervention research with children in clinical, public health, and other contexts. RESULTS: As illustrated by the evidence presented in this review, there are numerous reasons (biological, psychological, and social), opportunities (school and community, health care, and family settings), and approaches (nonintervention and intervention) to understand and impact behavior change in children's diet and nutrition and weight and physical activity. CONCLUSIONS: Further development and evaluation of behavioral science intervention protocols conducted with children are necessary to understand the efficacy of these approaches and their public health impact on proximal and distal cancer, cancer-related, and chronic disease outcomes before diffusion. It is clear that more attention should be paid to early life and early developmental phases in cancer prevention.     

Pain and Effusion and Quadriceps Activation and Strength

Context:

Quadriceps dysfunction is a common consequence of knee joint injury and disease, yet its causes remain elusive.

Objective:

To determine the effects of pain on quadriceps strength and activation and to learn if simultaneous pain and knee joint effusion affect the magnitude of quadriceps dysfunction.

Design:

Crossover study.

Setting:

University research laboratory.

Patients or Other Participants:

Fourteen (8 men, 6 women; age = 23.6 ± 4.8 years, height = 170.3 ± 9.16 cm, mass = 72.9 ± 11.84 kg) healthy volunteers.

Intervention(s):

All participants were tested under 4 randomized conditions: normal knee, effused knee, painful knee, and effused and painful knee.

Main Outcome Measure(s):

Quadriceps strength (Nm/kg) and activation (central activation ratio) were assessed after each condition was induced.

Results:

Quadriceps strength and activation were highest under the normal knee condition and differed from the 3 experimental knee conditions (P < .05). No differences were noted among the 3 experimental knee conditions for either variable (P > .05).

Conclusions:

Both pain and effusion led to quadriceps dysfunction, but the interaction of the 2 stimuli did not increase the magnitude of the strength or activation deficits. Therefore, pain and effusion can be considered equally potent in eliciting quadriceps inhibition. Given that pain and effusion accompany numerous knee conditions, the prevalence of quadriceps dysfunction is likely high.Key Words: arthrogenic muscle inhibition, central activation failure, voluntary activation, muscles

Key Points

• Knee pain and effusion resulted in arthrogenic muscle inhibition and weakness of the quadriceps.
• The simultaneous presence of pain and effusion did not increase the magnitude of quadriceps dysfunction.
• To reduce arthrogenic muscle inhibition and improve muscle strength, clinicians should employ interventions that target removing both pain and effusion.

Quadriceps weakness is a common consequence of traumatic knee joint injury^1,2 and chronic degenerative knee joint conditions.^3,4 Arthrogenic muscle inhibition (AMI), a neurologic decline in muscle activation, results in quadriceps weakness and hinders rehabilitation by preventing gains in strength.⁵ The inability to reverse AMI and restore muscle function can lead to decreased physical abilities,⁶ biomechanical deficits,⁷ and possibly reinjury.⁵ Furthermore, researchers^8,9 have suggested that quadriceps weakness resulting from AMI may place patients at risk for developing osteoarthritis in the knee. In light of the substantial influence of quadriceps AMI on these clinically relevant outcomes, we need to improve our understanding of the factors that contribute to this neurologic decline in muscle activity so efforts to target and reverse it can be implemented and gains in strength can be achieved more easily.Joint injury and disease are accompanied by numerous sequelae (ie, pain, swelling, tissue damage, inflammation), so ascertaining which one ultimately leads to neurologic muscle dysfunction is difficult. Whereas a joint effusion can result in AMI,^10–12 the effects of pain are less understood despite many clinicians attributing AMI to pain. Using techniques that introduce knee pain without accompanying injury may provide insights into the role of pain in eliciting AMI.The degree of knee joint damage may play a role in the quantity of AMI that manifests. Hurley et al^13,14 demonstrated that quadriceps AMI, measured using an interpolated-twitch technique, was greater in patients with extensive traumatic knee injury (eg, fractured tibial plateau, ruptured medial collateral ligament, and medial meniscectomy) than patients with isolated joint trauma (ie, isolated anterior cruciate ligament [ACL] rupture). Similarly, patients with more knee joint symptoms (ie, greater number of symptoms and increased severity of symptoms) may present with greater magnitudes of quadriceps inhibition. Recently, investigators¹⁵ have suggested that patients with more pain display less quadriceps strength, supporting this tenet. Given that effusion and pain often present simultaneously with joint injuries and diseases, such as ACL injury and osteoarthritis, examining both the isolated and cumulative effects of these sequelae appears warranted to determine if they influence the magnitude of muscle inhibition.Experimental joint-effusion and pain models are safe and effective experimental methods that allow for the isolated examination of their effects on muscle function. The effusion model, whereby sterile saline is injected directly into the knee joint capsule,⁷ produces a clinically relevant magnitude of the joint effusion that may be present with traumatic injury. Effusion is thought to activate group II afferents responding to stretch or pressure,^16–18 which in turn may facilitate group Ib interneurons and result in quadriceps AMI.⁵ The pain model involves injecting hypertonic saline into the infrapatellar fat pad to produce anteromedial knee pain similar to that described in patients with patellofemoral pain syndrome.¹⁹ Pain is considered to initiate AMI through activation of group III and IV afferents that act as nocioceptors to signal damage or potential damage to joint structures.^16–18 The firing of these afferents then may lead to facilitation of group Ib interneurons, the flexion reflex, or the gamma loop, ultimately resulting in quadriceps inhibition.²⁰ Thus, these models allow us to create symptoms that are associated with knee injury and have the added benefit of providing a way to examine their effects in isolation.Therefore, the purpose of our study was to determine the effects of pain on quadriceps strength and activation and to learn if simultaneous pain and knee joint effusion would affect the magnitude of quadriceps dysfunction. We hypothesized that pain alone would result in quadriceps inhibition and that the magnitude of inhibition would be greater when effusion and pain were present simultaneously.     

Postinfectious immunodeficiency and autoimmunity: pathogenic and clinical values and implications

Autoimmunity is still a mystery of clinical immunology and medicine as a whole. The etiology and pathogenesis of autoimmune disorders remain unclear and, thus, are assessed as a balance between hereditary predisposition, triggering factors and the appearance of autoantibodies and/or self-reactive T cells. Among the immunological armamentarium, molecular mimicry, based on self-reactive T- and B-cell activation by cross-reactive epitopes of infectious agents, is of special value. Hypotheses regarding the possible involvement of molecular mimicry in the development of postinfectious autoimmunity are currently very intriguing. They provide new approaches for identifying etiological agents that are associated with postinfectious autoimmunity, paired microbial- and tissue-linked epitopes targeted for autoimmune reaction determination, postinfectious autoimmunity pathogenesis recognition and specific prevention, and therapy for autoimmune disorder development.     

Beta-endorphin and drug-induced reward and reinforcement

Although drugs of abuse have different acute mechanisms of action, their brain pathways of reward exhibit common functional effects upon both acute and chronic administration. Long known for its analgesic effect, the opioid beta-endorphin is now shown to induce euphoria, and to have rewarding and reinforcing properties. In this review, we will summarize the present neurobiological and behavioral evidences that support involvement of beta-endorphin in drug-induced reward and reinforcement. Currently, evidence supports a prominent role for beta-endorphin in the reward pathways of cocaine and alcohol. The existing information indicating the importance of beta-endorphin neurotransmission in mediating the reward pathways of nicotine and THC, is thus far circumstantial. The studies described herein employed diverse techniques, such as biochemical measurements of beta-endorphin in various brain sites and plasma, and behavioral measurements, conducted following elimination (via administration of anti-beta-endorphin antibodies or using mutant mice) or augmentation (by intracerebral administration) of beta-endorphin. We suggest that the reward pathways for different addictive drugs converge to a common pathway in which beta-endorphin is a modulating element. beta-Endorphin is involved also with distress. However, reviewing the data collected so far implies a discrete role, beyond that of a stress response, for beta-endorphin in mediating the substance of abuse reward pathway. This may occur via interacting with the mesolimbic dopaminergic system and also by its interesting effects on learning and memory. The functional meaning of beta-endorphin in the process of drug-seeking behavior is discussed.     

PTEN与信号转导及肿瘤

ＴＥＮ[1] (ｐｈｏｓｐｈａｔａｓｅａｎｄｔｅｎｓｉｎｈｏｍｏｌｏｇｙｄｅｌｅｔｅｄｏｎｃｈｒｏｍｏｓｏｍｅｔｅｎ)又名ＭＭＡＣ1 [2 ] (ｍｕｔａｔｅｄｉｎｍｕｔｉｐｌｙａｄａｎｃｅｄｃａｎｃｅｒ 1 )和ＴＥＰ1 [3 ] (ＴＧＦ -βｒｅｇｕｌａｔｅｄａｎｄｅｐｉｔｈｅｌｉａｌｃｅｌｌ -ｒｉｃｈｅｄｐｈｏｓｐｈａｔａｓｅ 1 ) (以下均称为ＰＴＥＮ) ,是 1 997年由 3个研究小组先后发现的一个具有双特异磷酸酶活性的抑癌基因。ＰＴＥＮ基因异常广泛存在于人类多种恶性肿瘤 ,如恶性神经胶质瘤、前列腺癌、子宫内膜癌、黑色素瘤等…     

Tobacco and alcohol and the risk of head and neck cancer

Summary We carried out two case-control studies on the relative risk of head and neck cancer in association with tobacco and alcohol consumption. The first study carried out at the ENT Department of the University hospitals of Heidelberg and Giessen (FRG) comprised 200 male patients with squamous cell cancer of the head and neck and 800 control subjects matched for sex, age, and residential area (1:4 matching design). Of the tumour patients, 4.5% had never smoked, in contrast to 29.5% of the control group. The average tobacco and alcohol consumption of the patients was approximately twice as high as in the control subjects. The highest alcohol and tobacco consumption was observed in patients suffering from oropharyngeal cancer. Tobacco and alcohol increased the risk of head and neck cancer in a dose-dependent fashion and acted as independent risk factors. In heavy smokers (> 60 pack-years) a relative risk of 23.4 (alcohol adjusted) was calculated. Combined alcohol and tobacco consumption showed a synergistic effect. The risk ratio increased more in a multiplicative than in an additive manner. Oral and laryngeal cancer were associated with the highest tobacco-associated risk values. The highest ethanol-associated risk values were associated with oropharyngeal and laryngeal cancer. The second study was carried out at the ENT Department of the University of Heidelberg on 164 males with squamous cell carcinoma of the larynx and 656 control subjects matched for sex, age and residential area (1:4 matching design). Of the cases, 4.2% had never smoked, compared with 28.5% of the control subjects. The risk of laryngeal cancer by tobacco consumption was dose dependent, reaching a maximum value of 9.1 (adjusted for alcohol) for a consumption of more than 50 tobacco-years (TY). The relative risk of laryngeal cancer associated with alcohol intake was also dose dependent, reaching a value of 9.0 (adjusted for tobacco) for a mean daily consumption of more than 75 g alcohol. An analysis of subsite specific risks showed that heavy smokers (> 50 TY) carried a nearly ten times higher risk of supraglottic cancer than of glottic cancer. The risk of supraglottic cancer from alcohol consumption was also higher than that of glottic cancer.     

Muscle strength and serum testosterone,cortisol and SHBG concentrations in middle-aged and elderly men and women

Forty healthy males (M) and females (F) divided into two different age groups i.e. M50 years (range 44–57; n= 9), F50 years (range 43–54; n= 9), M70 years (range 64–73; n= 11) and F70 years (range 63–73; n= 11) volunteered as subjects for examination of muscle cross-sectional area (CSA) and maximal voluntary isometric force production characteristics of the leg extensor muscles and serum androgen and sex hormone binding globulin (SHBG) concentrations. The CSA in the male groups was greatly larger (P < 0.01) than in the female groups and both elderly groups demonstrated slightly (n.s.) smaller values in the CSA than the two middle-aged groups. Maximal force of 2854 ± 452 N in M50 was greater (P < 0.05) than that of 2627 ± 752 N recorded for F50 as well as the force of 2787 ± 843 in M70 was greater (P < 0.001) than that of 1849 ± 295 recorded for F70. The force between F50 and F70 differed significantly (P < 0.05) from each other. The maximal rate of force production in M50 was greater (P < 0.01) than in F50 as well as in M70 greater (P < 0.001) than in F70. Both middle-aged groups demonstrated greater (P < 0.05) values than the respective elderly groups of the same sex. The individual values in the CSA correlated with the values in maximal force both in the middle-aged subjects (r= 0.66; P < 0.01) and in the elderly subjects (r= 0.69; P < 0.01). The mean concentration of serum testosterone in M50 was slightly (n.s.) greater than in M70 and in F50 significantly (P < 0.05) greater than in F70. Serum SHBG levels were lower in the males (P < 0.01) than in the females and serum testosterone/SHBG ratio in M70 and in F70 were lower (P < 0.05) than in M50 and in F50, respectively. In the females significant positive correlations were observed between the individual values in serum testosterone concentration and the values both in the CSA (r= 0.46; P < 0.05) and in maximal force (r= 0.62; P < 0.01) as well as between serum testosterone/SHBG ratio and both the CSA (r= 0.55; P < 0.05) and maximal force (r= 0.68; P < 0.01). The present results imply that the decreasing basal level of blood testosterone over the years in aging people, especially in females, may lead to decreasing anabolic effects on muscles thus having an association with age-related declines in the maximal voluntary neuromuscular performance capacity in aging people.     

海洛因成瘾与学习记忆

海洛因成瘾是我国发病最高,危害最大的一种成瘾性疾病,而其中枢机制则是解决临床预防和治疗的关键,至今仍不清楚。既往工作表明,学习记忆功能在海洛因成瘾的中枢机制中居于重要的中心环节。本文在总结既往海洛因成瘾研究工作基础上联系学习记忆功能,试图从系统整合层次分析相关领域研究工作的不足和今后工作的发展方向。